Abstract
Oxidative stress is critically involved in a variety of diseases. Reactive oxygen species (ROS) are highly toxic molecules that are generated during the body's metabolic reactions and can react with and damage some cellular molecules such as lipids, proteins, or DNA. Liver is an important target of the oxidative stress because of its exposure to various prooxidant toxic compounds as well as of its metabolic function and ability to transform some xenobiotics to reactive toxic metabolites (as ROS). To investigate the processes of liver injuries and especially liver oxidative damages there are many experimental models, some of which we discuss further.
Highlights
Oxidative stress is an imbalance between the production and scavenging of reactive oxygen and nitrogen species (ROS and RNS) and free radicals that can induce lipid peroxidation, DNA fragmentation, and protein oxidation [1]
Liver plays a pivotal role in the regulation of various physiological processes in the body such as carbohydrate metabolism and storage, fat metabolism, bile acid synthesis, and so forth besides being the most important organ involved in the detoxification of various drugs as well as xenobiotics in our body [3]
We found that Reactive oxygen species (ROS), produced by CCl4, decrease the activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) [18], and the activities of some drug metabolizing enzymes such as CYP2E1 and CYP3A, involved in their production [15]
Summary
Oxidative stress is an imbalance between the production and scavenging of reactive oxygen and nitrogen species (ROS and RNS) and free radicals that can induce lipid peroxidation, DNA fragmentation, and protein oxidation [1]. Hepatic injury through carbon tetrachloride induced lipid peroxidation is well known and has been extensively used in the experimental models to understand the cellular mechanisms behind oxidative damage and further to evaluate the therapeutic potential of drugs and dietary antioxidants [8]. CCl4 is activated by cytochrome CYP2E1, CYP2B1, or CYP2B2, and possibly CYP3A, to form the trichloromethyl radical, CCl3∗ [9] This radical can bind to cellular molecules (nucleic acid, protein, lipid), impairing crucial cellular processes such as lipid metabolism, with the potential outcome of fatty degeneration (steatosis) [10]. Many other drugs as isoniazide, amiodarone, and valproic acid as well as widely used and abused substances as nicotine and cocaine damage liver cells by producing toxic ROS Because of their widespread consumption, they are used as experimental models of liver injuries
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